The Effect and the Mechanism of Action of High Frequency Electrical Stimulation of Subthalamic Nucleus on Status Epilepticus Induced by Lithium-Pilocarpine of Rat.
- Author:
Young Min SHON
1
;
Soung Kyeong PARK
;
Yeong In KIM
;
Dong Won YANG
;
Yong Soo SHIM
;
Beum Saeng KIM
Author Information
1. Department of Neurology, College of Medicine, The Catholic University of Korea, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Deep brain stimulation;
Subthalamic nucleus, Fos immunoreactivity;
Lithium-pilocarpine induced status epilepticus
- MeSH:
Animals;
Deep Brain Stimulation;
Electric Stimulation*;
Epilepsy;
Immunohistochemistry;
Pilocarpine;
Rats*;
Seizures;
Status Epilepticus*;
Subthalamic Nucleus*;
Thalamic Nuclei
- From:Journal of Korean Epilepsy Society
2005;9(1):10-16
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVES: Deep brain stimulation (DBS) of subthalamic nuclei (STN) is one of the current modalities of refractory epilepsy, but its exact mechanism and route of action have not been elucidated yet. We investigated the effect of STN stimulation on the development and propagation of seizures in the rats with lithium-pilocarpine induced status epilepticus in its functional anatomy. METHODS: Both pilocarpine injection and high frequency stimulation on STN (HFSSTN) were provided to rats (STN group, n=12), but pilocarpine injection with no stimulation was done on the sham group (n=8). The latency to first discrete ictal discharges and the latency to status epilepticus (SE) were analyzed and the electrical stimulation lasted for 30, 60, 90, 120 minutes after its first discrete spikes. After stimulation, the rats were immediately decapitated for immunohistochemistry and histologic examination. RESULTS: Both the latency to first discrete ictal discharges and the latency to the onset of SE were delayed in the STN group than in the sham group. The latency to the first SE was also more delayed in the STN group (42.7+/-7.9 min) than in the sham group (p<0.05). Remarkably, there was marked Fos immunoreactivity (FIR) on the reticular thalamic nuclei in the STN group, but not in the sham group. CONCLUSIONS: Increased FIR in the reticular thalamic nuclei during HFSSTN suggested that the facilitation of the inhibitory thalamic output prevented generalized motor seizure behavior. We assume that HFSSTN has a pivotal role in the suppression or progression to SE, but cannot prevent seizure onset.
